When thsScer\UAS.cSa is expressed in the entire mesoderm under the control of Scer\GAL4twi.PG the migrating longitudinal visceral muscle (LVM) precursors fail to divide into two bilateral streams as in wild type and occupy areas around the midline. The cells are oriented more randomly and migration is much less directional compared to wild type. A later stages partial loss of LVM cells is seen. After germ cell retraction none of the remaining LVMs have migrated to the anterior trunk visceral mesoderm, and are instead retained in the posterior third of the embryo, where they form irregular aggregates of fibers.
Expression of thsScer\UAS.cSa in the dorsal ectoderm under the control of Scer\GAL4pnr-MD237 causes most of the longitudinal visceral muscle (LVM) founder cells to take a more lateral migration path, rather than their usual route towards the trunk visceral mesoderm (TVM). Many LVM founders target towards the pericardial and somatic muscle progenitors in the dorsal mesoderm, often surrounding them and sending extensions toward the ectoderm. Many of these laterally targeted cells continue to migrate in anterior directions and successfully reach the anterior TVM through this alternative route. LVM fibres are found both underneath the dorsal ectoderm as well as around the midgut as in wild type.
Expression of thsScer\UAS.cSa in the trunk visceral mesoderm (TVM) under the control of Scer\GAL4bap.3 has no effect on the direction or distance of longitudinal visceral muscle founder cell migration in the stage 12/13 embryo.
Expression of thsScer\UAS.cSa under the control of Scer\GAL469B has little or no effect on mesoderm monolayer formation in the embryo following gastrulation.
Embryos expressing thsScer\UAS.cSa under the control of Scer\GAL4twi.PG form most mesoderm lineages, including the pharyngeal muscles and the hindgut musculature. The ventral oblique muscles are either absent or unable to extend into ventral regions. Embryos expressing thsScer\UAS.cSa under the control of Scer\GAL469B show a substantial expansion of pericardial cell specification.
Df(2R)BSC25, Scer\GAL4sim.P3.7, pyrUAS.cKa, thsUAS.cSa has abnormal cell migration | embryonic stage phenotype
Df(2R)BSC25, Scer\GAL4fkh.PH, thsUAS.cSa has decreased cell number | embryonic stage phenotype
Df(2R)BSC25, Scer\GAL4fkh.PH, thsUAS.cSa has abnormal cell migration | embryonic stage phenotype
Df(2R)BSC25, Scer\GAL4bap.3, thsUAS.cSa has abnormal cell migration | embryonic stage phenotype
thsUAS.cSa/Scer\GAL4elav-C155 partially rescues Df(2R)BSC25
thsUAS.cSa/Scer\GAL4VGlut1-OK371 partially rescues Df(2R)BSC25
thsUAS.cSa/Scer\GAL4Ntan1-Mz97 partially rescues Df(2R)BSC25
thsUAS.cSa/Scer\GAL4twi.PG partially rescues Df(2R)BSC259/Df(2R)BSC25
thsUAS.cSa/Scer\GAL4pnr-MD237 partially rescues Df(2R)BSC259/Df(2R)BSC25
thsUAS.cSa/Scer\GAL4bap.3 partially rescues Df(2R)BSC259/Df(2R)BSC25
thsUAS.cSa/Scer\GAL448Y partially rescues Df(2R)BSC259/Df(2R)BSC25
Expression of thsScer\UAS.cSa under the control of either Scer\GAL4elav-C155 or Scer\GAL4VGlut-OK371 partially rescues infiltration of astrocyte processes into the neuropil in Df(2R)BSC25 embryos, however, migration of the ventral-most astrocyte is not rescued.
Expression of thsScer\UAS.cSa under the control of Scer\GAL4tub.PU in single neurons in the central nervous system (using the RN2-FLP clone system) robustly rescues infiltration of the neuropil by astrocyte processes in Df(2R)BSC25 embryos, with infiltration being seen even some distance beyond the volume covered by Diap1[+] neurites.
Expression of thsScer\UAS.cSa under the control of Scer\GAL4Mz97 partially rescues infiltration of astrocyte processes into the neuropil in Df(2R)BSC25 embryos, however, migration of the ventral-most astrocyte is not rescued. In addition, ectopic astrocyte projections are seen along the dorsal central nervous system surface and nerves and astrocyte cell bodies are displaced to dorsal and lateral positions.
Expression of thsScer\UAS.cSa in the entire mesoderm under the control of Scer\GAL4twi.PG fails to rescue the long-range longitudinal visceral muscle (LVM) founder cell migration defects seen in Df(2R)BSC25/Df(2R)BSC259 (FGF8 null) mutant embryos. However founder cell survival is partially rescued.
Expression of thsScer\UAS.cSa in the dorsal ectoderm under the control of Scer\GAL4pnr-MD237 partially rescues the long-range longitudinal visceral muscle (LVM) founder cell migration defects seen in Df(2R)BSC25/Df(2R)BSC259 (FGF8 null) mutant embryos. Whilst some cells take the route seen in wild type, most of the cells take a more lateral migration path under the dorsal ectoderm. Far fewer cells migrate along the trunk visceral mesoderm (TVM).
Expression of thsScer\UAS.cSa in the trunk visceral mesoderm (TVM) under the control of Scer\GAL4bap.3 significantly rescues the long-range longitudinal visceral muscle (LVM) founder cell migration defects seen in Df(2R)BSC25/Df(2R)BSC259 (FGF8 null) mutant embryos, although the migrating cells are arranged in a less orderly fashion. Founder cell survival is also rescued. The morphogenesis of the LVMs proceeds relatively normally.
Expression of thsScer\UAS.cSa in the endoderm under the control of Scer\GAL448Y significantly rescues the long-range longitudinal visceral muscle (LVM) founder cell migration defects seen in Df(2R)BSC25/Df(2R)BSC259 (FGF8 null) mutant embryos, although the migrating cells are arranged in a less orderly fashion. Founder cell survival is also rescued. The morphogenesis of the LVMs proceeds relatively normally.
Expression of thsScer\UAS.cSa under the control of Scer\GAL4sim.P3.7 does not rescue mesoderm spreading in Df(2R)BSC25 embryos and in mesoderm cells tend to pool at the ventral midline.
Expression of thsScer\UAS.cSa under the control of Scer\GAL4zen.Kr.PF partially rescues mesoderm spreading in Df(2R)BSC25 embryos.
